Embargo expired: 5/27/2010 12:00 AM EDT
Source Newsroom: Environmental Health Perspectives (NIEHS)
Newswise — Traffic-related air pollution, known to raise the risk for cardiovascular disease, may also increase the risk of developing type 2 diabetes in women. Low-grade inflammation may contribute to the higher incidence of type 2 diabetes in women exposed to air pollution, according to German researchers.
Published online May 27 ahead of print in the peer-reviewed journal Environmental Health Perspectives (EHP), the study comprised German women living in highly polluted industrial areas and in rural regions with less pollution. The researchers analyzed data from 1,775 women who were 54 or 55 years old when they enrolled in the study in 1985. Between 1990 and 2006, 187 participants were diagnosed with type 2 diabetes, which often starts in middle age. Air pollution data from monitoring stations and emission inventories run by local environmental agencies were used to estimate each woman's average exposure levels.
Exposure to components of traffic pollution, particularly nitrogen dioxide (NO2) and soot in ambient fine particulate matter (PM), was significantly associated with a higher risk of type 2 diabetes. An increase in NO2 or PM corresponding to the difference between exposure at the 75th percentile and exposure at the 25th percentile was associated with a 15–42% higher risk of type 2 diabetes. Living within 100 meters of busy roadways more than doubled the diabetes risk.
Measurements of C3c, a blood protein and marker for subclinical inflammation, predicted the elevated diabetes risk. Only women with the highest C3c levels at enrollment had an increased risk for type 2 diabetes related to traffic pollution during the 16-year follow-up period. Just how C3c might affect diabetes remains unknown. Immune cells in the airways may first react with air pollutants, setting off a widespread chronic inflammatory response, which in turn may make individuals more susceptible to developing diabetes.
Although the study focuses only on women, study leader Wolfgang Rathmann says, "We have no reason to assume sex differences in the association between air pollution and diabetes risk, but we do not have data on this issue."
To the authors' knowledge, this is the first population-based study to reveal a statistically significant association between traffic-related air pollution and type 2 diabetes. Previous epidemiologic research shows that city dwellers have a higher prevalence of diabetes than do rural residents, especially in developing countries undergoing rapid industrialization. Changes in diet and physical activity and resulting increases in obesity are believed to be the primary culprits. These changes, however, do not totally explain the increased diabetes risk. The results of the current study suggest traffic-related air pollutants may be an unidentified environmental factor related to the development of type 2 diabetes.
Other studies have reported that people with diabetes are more vulnerable to pollution-related cardiovascular disease. Air pollutants can cause low-grade inflammation, insulin resistance, and impaired glucose metabolism. Additionally, C3c is a risk factor for diabetes, and C3c levels are higher in individuals living in highly polluted areas. The latest findings further support the role of traffic air pollutants and low-grade inflammation in diabetes risk.
Other authors of the study are Ursula Krämer, Christian Herder, Dorothea Sugiri, Klaus Strassburger, Tamara Schikowski, and Ulrich Ranft. The full article, "Traffic-Related Air Pollution and Incident Type 2 Diabetes: Results from the SALIA Cohort Study," is available on the EHP website at http://ehponline.org/article/info:doi/10.1289/ehp.0901689.
EHP is published by the National Institute of Environmental Health Sciences, part of the U.S. Department of Health and Human Services. EHP is an open-access journal. More information is available online at http://www.ehponline.org/. Brogan & Partners Convergence Marketing handles marketing and public relations for the publication and is responsible for creation and distribution of this press release.
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